A re-appraisal of the role of layer VI of the visual cortex in the generation of cortical end inhibition.

These experiments examine the effect of blockade of layer VI of the cat striate cortex on the length tuning of hypercomplex cells in the overlying layers II, III and IV. It has previously been suggested that local inactivation of layer VI results in the complete loss of length selectivity in all hypercomplex cells in layers II, III and IV above the blocked region, by removal of an inhibitory mechanism within layer IV, driven from layer VI. However, we have found that, using iontophoretic application of the inhibitory substance GABA to block the activity of layer VI, 29% of hypercomplex cells were unaffected by blockade of the underlying layer VI. The predominant effect on hypercomplex cells was a reduction in visual responsiveness, seen in 71% of cells, with responses reduced on average by 43%. In 50% of these cells (35% of the population) this reduction was apparently specific to responses to the optimum bar length; responses to longer stimuli were unaffected. Iontophoretic application of the potent GABAA analogue muscimol in layer VI showed a similar spectrum of effects on hypercomplex cells. In these cases, however, the cortical blockade was slowly increased to encompass the recorded cell. In each case, any decreases in length selectivity were also the result of a decreased visual responsiveness. Thus, decreases in length selectivity seen when using either GABA or muscimol were almost exclusively the result of decreased responsiveness to the optimal length of bar stimulus, rather than an increase in response to non-optimal, long stimuli. This suggests the loss of a facilitatory influence from layer VI to layer IV, rather than the loss of inhibition.